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Query: UMLS:C0086543 (
cataract
)
29,165
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
It was established earlier that the maintenance of rats on a galactose-rich diet induced in rat liver a sequental induction of enzymes, converting galactose to glucose (galactokinase, galactoso-1-phosphaturidytransferase and uridyndiphosphogalactose-
4-epimerase
); this was followed by the repression of these enzymes. Against the background of the enzyme repression, the continuation of galactose treatment leads to the development of galactosemia symptoms; cataracts, liver lesions growth retardation. Animals with the increased susceptibility to galactose were found in population of Wistar rats; in these animals rapidly developing enzyme induction is followed by sharp repression of enzymes of the galactose metabolism and in them cataracts appear 17-19 days after the start of feeding a galactose-rich diet. A part of the population is resistant to the galactosemic effect of galactose and in these animals cataracts develope only 40-44 days after the beginning of the galactose feeding. By inbreeding of individuals extremely susceptible to galactose and those resistant to it, new substrains of rats were obtained. It is found that in the rats of the galactose-susceptible substrain a number of galactosemic features develope spontaneously and that these features are inheritable. Thus, 85% of the animals of the age of 2.5-6 months have
cataract
, lens opacities and other lens impairments. In the galactose-resistant substrain no cataracts or lens opacities develope and only slight changes of the lens are observed in 15% of the animals. In the susceptible substrain other features characteristic of galactosemia occur: an increase in the size of thymus, spleen and liver. It is established that in 3.5-5 month old rats of the galactose-susceptible substrain the galactoso-1 phosphaturidyltransferase activity in blood hemolysates is 15 times lower than in rats of galactose-resistant substrain, and in liver the activity of this enzyme is 1.4 times lower. The activity of liver galactokinase and uridyldiphosphogalactose-
4-epimerase
is slightly higher in rats of galactose-susceptible substrain than in galactose-resistant 1.
...
PMID:[Development of a rat subline with symptoms of hereditary galactosemia and study of its biochemical characteristics]. 124 Aug 12
In addition to the already recognized metabolic diseases which have been associated with
cataract
formation, e.g. galactosaemia, galactokinase deficiency, Lowe's syndrome and diabetes, several other disorders can also lead to the development of cataracts. They are sorbitol dehydrogenase deficiency, uridine diphosphate galactose-
4-epimerase
deficiency, marginal maternal transferase and galactokinase deficiency, galactitol and sorbitol accumulation of unknown origin, heterozygosity for galactosaemia and galactokinase deficiency as well as the carrier state for Lowe's syndrome. In this review these metabolic disorders have been divided into five groups according to the age at the first appearance of lens clouding and the possible means of treatment have been discussed.
...
PMID:Cataract and metabolic disease. 212 17